The field of the invention relates to methods for treating and/or preventing cell death and organ damage in a subject following an ischemic event. In particular, the field of the invention relates to methods for treating and/or preventing cell death and organ damage in a subject following an ischemic event by administering an iron chelator to the subject.
Heart failure is a common disorder and our current treatments are limited. In the past few years, several studies have suggested that giving iron supplementation may be beneficial in certain patients with iron deficiency and heart failure. However, these studies have only shown an improvement in symptoms in patients with heart failure and studies on the improvement of cardiac function in these patients is limited. Furthermore, earlier studies had indicated that an increase in mitochondrial iron in the heart is associated with cardiomyopathy. Iron is an essential molecule for normal cellular physiology. However, in excess iron is also a source of oxidative stress and cellular damage. Other studies had shown that iron chelators, which function by chelating and reducing cellular iron, reduce cardiac damage only in some cases, and some studies had shown no benefit of treatment with these molecules. Based on these prior art, the present inventors hypothesized that a reduction in mitochondrial iron would be protective against the development of heart failure. Here, the inventors show in tissue culture and in animal models that a reduction in mitochondrial iron is protective against ischemic injury in the heart and the development of cardiomyopathy.